
KRAS-Mutant Atlas at a glance
- Models
- 50+ KRAS-mutant
- Indications
- NSCLC, CRC, pancreatic
- Reference arm
- Daraxonrasib
- Profiling
- Baseline to endpoint

KRAS-Mutant Atlas
A reference atlas of response, resistance and multi-omic profiling across 50+ KRAS-mutant patient-derived tumor models, each run under daraxonrasib, ready to compare your compound against.
Overview
Daraxonrasib was approved in August 2026 for previously treated metastatic pancreatic cancer, the first approval for a RAS(ON) inhibitor. KRAS-directed programs will now be asked how they compare, where they add benefit and whether they work where daraxonrasib has stopped working. Shrinkage against vehicle cannot answer those questions.
The atlas is a reference dataset built on that comparison. Panel models are profiled at baseline, under treatment and at endpoint, all under daraxonrasib. Your compound runs through the same profiling at the same timepoints, on the models you choose, so the readout is differentiation rather than activity.
The panel spans non-small cell lung, colorectal and pancreatic cancer, and includes models induced for resistance to daraxonrasib. Optional comparator arms, such as a second KRAS inhibitor or a chemotherapy standard, widen the frame where your development plan needs them.

Study depths
Your compound and a parallel daraxonrasib arm run on the models you select. Tumor growth inhibition and regression, read by clinically correlated modified RECIST, show where your asset beats, matches or trails the reference, by indication and mutation.
A subset of models induced for daraxonrasib resistance shows whether your compound holds where the reference has already failed.
Supports
Differentiation go or no-go
Choosing which indication first
Positioning after daraxonrasib

Get Started
Discover how surface expression correlates with treatment response.
Explore new target opportunities validated in real human tumors.
Assess the quality and interpretability of our data for your own programs.
Deliverables
Head-to-head response data
Tumor growth inhibition and regression for your compound and daraxonrasib on identical models and timepoints.
Resistance-model performance results
How your compound performs in models already resistant to daraxonrasib, reported model by model.
Matched baseline molecular profiles
Exome, transcriptome and proteomic data for every model in your study, each linked to its response.
Candidate response markers
Features that separate responders from non-responders, with the contrast and model subset behind each one.
Ranked combination hypotheses
Mechanism-backed combinations ranked by the resistance biology they target, ready for in vivo testing.
Methods and source data
Figures, tables and methods behind each conclusion, with the underlying data available on request.

Why now
FAQ
Related pages
Data platform
Every way to work with the data, from target packages to licensed cohorts.
Cell-surface proteomics
How the surface resistance markers in the atlas are measured and validated.
KRAS preclinical platform
In vivo KRAS models and study designs beyond the daraxonrasib benchmark.
Mouse clinical trials
Cohort-scale in vivo studies that run your compound across many models at once.

Plan a study
Tell us the compound class or mechanism, the indications and mutations you are prioritizing, and which depth of study you have in mind. If the compound is confidential, describe the class and we will put a CDA in place before details are shared.
A scientist replies to every request personally
Available panel models noted in the reply
CDA handled before any compound detail is shared